Although downregulation of Foxp3 and high-affinity IL-2 receptor CD25 expression by Tregs had been reported before in various infection- or autoimmune diseases-associated inflammatory milieus (37–39), to the best of our knowledge we are the first to demonstrate that the inflammation-driven downregulation of Foxp3 and Il2ra could persist far beyond the resolution of the inflammation. The gene discussed is FOXP3; the disease is infection.